Salicylates induce antibiotic resistance in E. coli via at least two pathways: one dependent upon the multiple antibiotic resistance locus, mar, and the other by a mar independent mechanism. We had previously isolated a number of insertion mutants in a strain deleted for the mar region that failed to exhibit increased resistance to nalidixic acid in the presence of salicyl alcohol. The location of the insertion in three of these strains has now been identified. Two are independent insertions in uvrD, the gene that encodes the helicase required for repair following DNA damage. The third is located in pgm, the gene that encodes phosphoglucomutase. We have traced the failure of salicylates to induce antibiotic resistance in the pgm strains to a deficiency for glucose-1-P required for synthesis of the lipopolysaccacharides of the outer membrane. While others have reported that a 7.8 kbp mar region is necessary for the Mar phenotype, we have demonstrated that only the promoter (<150 bp in length), the marR and the marA genes are required. Salicylate may interact directly with the marR protein since upon removal of salicylate, induction of the pathway ceases immediately. An expression vector carrying a functional MarR gene has been isolated and purification of marR is underway. An expression vector carrying a putative marA gene has also been isolated. Goal: To identify the mechanisms of salicylate induction of antibiotic resistance in the mar and non-mar pathways.